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J W Guzek

Publications and source records attributed to J W Guzek.

At least 73 records · Page 4Linked to original sources
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Intracerebroventricular insulin affects the neurohypophysial vasopressin content in euhydrated and dehydrated rats.

Rats euhydrated or dehydrated for four days were given intracerebroventricular insulin once daily in a dose of 100 ng (not affecting blood sugar level). In euhydrated rats, insulin decreased significantly the neurohypophysial vasopressin content. In dehydrated animals the neurohypophysial content depleted by deprivation of water could be further reduced by intracerebroventricular treatment with insulin. These results may suggest a possible regulatory role of brain insulin in the mechanisms of vasopressin release.

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The vasopressin content in the neurohypophysis under conditions of intracerebroventricular beta-adrenergic blockade in euhydrated and dehydrated rats.

Rats dehydrated for up to 8 days were given propranolol hydrochloride into the left brain ventricle in a daily dose of 10 micrograms. In euhydrated rats the single dose of propranolol diminished significantly the vasopressin content in neurohypophysis. In animals dehydrated for two days, the depletion of the neurohypophysial vasopressin storage was less marked under conditions of treatment with propranolol. At the fourth and eighth day of deprivation of water, propranolol did not modify the decrease of neurohypophysial vasopressin due to stimulation of osmodetectors.

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Studies on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis.

The effects of modified adrenergic transmission on the bioassayed storage of vasopressin and oxytocin in the hypothalamus and neurohypophysis under conditions of stress (cold or immobilization), disturbed water balance and pinealectomy are reviewed. Alpha-adrenergic mechanisms seem to be included in the response of vasopressinergic and oxytocinergic neurones to stress; on the other hand, impulses of osmoreceptor origin are of importance in regulatory processes affecting the functional response of these neurones to altered alpha-adrenergic transmission and also to melatonin. The beta-adrenergic (and, to some extent, also the alpha-adrenergic) transmission is probably involved in the neural mechanisms of the pineal-neurohypophysial relationship. Furthermore, a possible regulatory role of cholecystokinin in water metabolism and release of neurohypophysial hormones is suggested.

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The hypothalamic and neurohypophysial vasopressor and oxytocic content as influenced by alpha-adrenergic blockade in stressed rats.

The hypothalamic and neurohypophysial vasopressor and oxytocic content as influenced by alpha-adrenergic blockade in stressed rats. Acta physiol. pol., 1985, 36 (3): 193-200. The effects of phenoxybenzamine (PBA; an alpha-adrenergic blocker) on hypothalamic and neurohypophysial vasopressin and oxytocin were investigated in stressed rats. Immobilization resulted in a decrease of both vasopressor and oxytocic activities in the hypothalamus and neurohypophysis, whereas in rats, exposed to cold the vasopressin and oxytocin content in the hypothalamo-neurohypophysial system was increased. Under treatment with PBA the vasopressin and oxytocin content in the neurohypophysis was diminished in stressed (both immobilized and cold-exposed) rats when compared to respective groups of untreated animals subjected to appropriate kind of stress. The response of the vasopressinergic and oxytocinergic neurones seems, therefore, to be dependent on the type of stress. The alpha-adrenergic transmission is probably in some way involved in the mechanisms of modified neurohypophysial function in stressed animals.

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The hypothalamic and neurohypophysial vasopressin and oxytocin content under various states of adrenergic transmission in dehydrated and subsequently rehydrated rats.

Rats dehydrated for 8 days and subsequently rehydrated were given intracerebroventricularly (i.c.v.) methoxamine hydrochloride (MX) or dihydroergotamine methanosulphonate (DHE), each in a daily dose of 10 micrograms dissolved in 10 microliter of 0.9% sodium chloride. A single dose of MX injected to normally hydrated animals increased the release of hypothalamic and neurohypophysial vasopressin but did not affect significantly the oxytocic activity in the hypothalamus as well as in the neurohypophysis. Under conditions of dehydration MX did not influence the hypothalamic vasopressin content but it stimulated the neurohypophysial vasopressin depletion. On the contrary, MX distinctly inhibited the decrease of hypothalamic and neurohypophysial oxytocin content in dehydrated animals. In rehydrated animals MX restrained some what the renewal of hypothalamic vasopressin and oxytocin storage but intensified this process in the neurohypophysis. A single dose of DHE decreased the vasopressin content in the hypothalamus as well as the oxytocin content both in the hypothalamus and neurohypophysis. Under conditions of dehydration DHE stimulated the depletion of hypothalamic vasopressin and oxytocin. On the contrary, DHE strongly inhibited the depletion of oxytocin in the neurohypophysis of dehydrated rats. DHE restrained the renewal of hypothalamic vasopressin and oxytocin stores as well as intensified this process in the neurohypophysis of subsequently rehydrated rats.

Adrenergic Fibers↗
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Karol Klecki 1866-1931.

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Bacterial Infections↗
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The neurohypophyseal vasopressin content under conditions of inhibited synthesis of prostaglandins in euhydrated and dehydrated rats.

Rats euhydrated or dehydrated up to eight days were given intraperitoneally indomethacin (IM) twice daily in a dose of 0.2 mg/100 g of initial body weight. A single dose of IM injected to euhydrated animals did not affect the neurohypophyseal vasopressor activity; however, when administered repeatedly during four or eight days, IM increased significantly the neurohypophyseal vasopressor activity. Under conditions of severe dehydration (eight days of water deprivation) the known depletion of neurohypophyseal vasopressin store was not significantly affected by indomethacin. It is, therefore, suggested that impulses of osmoreceptor origin are of distinct importance in determining the function of vasopressinergic neurons under conditions of inhibited prostaglandin synthesis.

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